ArticleNature communications2016
LRRK2 regulates retrograde synaptic compensation at the Drosophila neuromuscular junction.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- The multifaceted interactions between Newcastle disease virus proteins and host proteins: a systematic review.Virulence · 2024Pooled it
- GARP Complex in Golgi Physiology.Sub-cellular biochemistry · 2026Review
- A retrograde, non-canonical integrated stress response cascade maintains synaptic strength under amino acid deprivation.Cell reports · 2025Article
- LRRK2 in Drosophila Melanogaster Model: Insights into Cellular Dysfunction and Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2025Review
- Genetic evidence for a functional association between Parkinson's disease proteins leucine-rich repeat kinase 2 andFrontiers in molecular neuroscience · 2025Article
- A glutamate receptor C-tail recruits CaMKII to suppress retrograde homeostatic signaling.Nature communications · 2022Article
- The emerging role of furin in neurodegenerative and neuropsychiatric diseases.Translational neurodegeneration · 2022Review
- Synaptic homeostats: latent plasticity revealed at the Drosophila neuromuscular junction.Cellular and molecular life sciences : CMLS · 2021Review
- Age-dependent degeneration of an identified adult leg motor neuron in aBiology open · 2020Article
- Defects in mRNA Translation in LRRK2-Mutant hiPSC-Derived Dopaminergic Neurons Lead to Dysregulated Calcium Homeostasis.Cell stem cell · 2020Article
- Dietary Amino Acids Impact LRRK2-Induced Neurodegeneration in Parkinson's Disease Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Identification of PP2A and S6 Kinase as Modifiers of Leucine-Rich Repeat Kinase-Induced Neurotoxicity.Neuromolecular medicine · 2020Article
- Sleep Spindles and Fragmented Sleep as Prodromal Markers in a Preclinical Model of LRRK2-G2019S Parkinson's Disease.Frontiers in neurology · 2020Article
- Origins of Parkinson's Disease in Brain Development: Insights From Early and Persistent Effects of LRRK2-G2019S on Striatal Circuits.Frontiers in neuroscience · 2020Review
- LRRK2 Biology from structure to dysfunction: research progresses, but the themes remain the same.Molecular neurodegeneration · 2019Review
- Glioblastoma cells vampirize WNT from neurons and trigger a JNK/MMP signaling loop that enhances glioblastoma progression and neurodegeneration.PLoS biology · 2019Article
- Inhalation of marijuana affectsBiology open · 2019Article
- Estimation of the Readily Releasable Synaptic Vesicle Pool at theBio-protocol · 2019Article
- The Muscle Is Not a Passive Target in Myasthenia Gravis.Frontiers in neurology · 2019Review
- Synapse-specific and compartmentalized expression of presynaptic homeostatic potentiation.eLife · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Parkinson's disease gene leucine-rich repeat kinase 2 (LRRK2) has been implicated in a number of processes including the regulation of mitochondrial function, autophagy and endocytic dynamics; nevertheless, we know little about its potential role in the regulation of synaptic plasticity. Here we demonstrate that postsynaptic knockdown of the fly homologue of LRRK2 thwarts retrograde, homeostatic synaptic compensation at the larval neuromuscular junction. Conversely, postsynaptic overexpression of either the fly or human LRRK2 transgene induces a retrograde enhancement of presynaptic neurotransmitter release by increasing the size of the release ready pool of vesicles. We show that LRRK2 promotes cap-dependent translation and identify Furin 1 as its translational target, which is required for the synaptic function of LRRK2. As the regulation of synaptic homeostasis plays a fundamental role in ensuring normal and stable synaptic function, our findings suggest that aberrant function of LRRK2 may lead to destabilization of neural circuits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.